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Abstract
Advances in neuroscience identified addiction as a chronic brain disease with strong
genetic, neurodevelopmental, and sociocultural components. We here discuss the circuit-
and cell-level mechanisms of this condition and its co-option of pathways regulating
reward, self-control, and affect. Drugs of abuse exert their initial reinforcing effects
by triggering supraphysiologic surges of dopamine in the nucleus accumbens that activate
the direct striatal pathway via D1 receptors and inhibit the indirect striato-cortical
pathway via D2 receptors. Repeated drug administration triggers neuroplastic changes
in glutamatergic inputs to the striatum and midbrain dopamine neurons, enhancing the
brain's reactivity to drug cues, reducing the sensitivity to non-drug rewards, weakening
self-regulation, and increasing the sensitivity to stressful stimuli and dysphoria.
Drug-induced impairments are long lasting; thus, interventions designed to mitigate
or even reverse them would be beneficial for the treatment of addiction.